Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.

He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.

By Jefferson Adams

Published on 06/10/2013

Researchers have known for some time that immunoglobulin G antibodies against deamidated gliadin peptides are about as accurate as tissue transglutaminase and endomysium autoantibodies in diagnosing celiac disease in adults. However, not much is known about their predictive value in infants with a suspected gluten enteropathy.

Celiac.com 06/10/2013 - Researchers have known for some time that immunoglobulin G antibodies against deamidated gliadin peptides are about as accurate as tissue transglutaminase and endomysium autoantibodies in diagnosing celiac disease in adults. However, not much is known about their predictive value in infants with a suspected gluten enteropathy.

A team of researchers recently set out to determine if antibodies to deamidated gliadin peptides could be an accurate predictor of celiac disease in infants.

To test whether deamidated gliadin immunoglobulin G antibodies are more reliable than traditional tests for screening celiac disease in infants, the researchers tested 65 children under 2 years of age for deamidated gliadin immunoglobulin G, tissue transglutaminase and endomysium immunoglobulin A, and gliadin immunoglobulins A and G. The group included 42 infants with malabsorption, along with 23 infants as control subjects.

Thirty-seven of the 42 children with malabsorption had deamidated gliadin antibodies, associated with tissue transglutaminase and endomysial antibodies in 33, and with gliadin immunoglobulins A and G in 21 and 29, respectively.

The team conducted intestinal biopsy in 34 of the 37 children who tested positive for deamidated gliadin antibodies. Thirty-two of the 34 showed villous atrophy consistent with celiac disease, while one of the remaining two had a Marsh 1 and the other showed normal mucosa. The control group showed only gliadin immunoglobulins A (4.3 %) and G (39.1 %).

The results showed that deamidated gliadin, tissue transglutaminase and endomysial antibodies were significantly more sensitive for celiac disease than gliadin immunoglobulins G and A.